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Background: Aim of this cross-sectional, multicentre study was to investigate associations of dialysis vintage time in haemodialysis (CKD5D) patients with oral health-related quality of life (OHRQoL) and dental and periodontal treatment need. Material and Methods: CKD5D patients were divided into subgroups according to dialysis vintage time in different dialysis centres in Germany. OHRQoL was assessed with oral health impact profile (OHIP-G14). Dental treatment need was classified as presence of carious lesions. Periodontal treatment need was defined as periodontal screening index score (PSI) 3-4. Results: In total, 190 participants were divided into the subgroups according to the time on CKD5D: 0 - 2 (n = 29), 3 - 5 (n = 35), 6 - 8 (n = 34), 9 - 12 (n = 29), 13 - 20 (n = 34) and >20 years (n = 29). The overall treatment need in the total cohort was 92% (dental 56%, periodontal 88%) with a total OHIP-G14 sum score of 4.17 [2; 0-5] without a significant correlation. Time on CKD5D was inversely correlated with the OHIP G14 score (p<0.01, R = -0.201). The pattern psychosocial impact was significantly associated with the dialysis duration (p<0.01) and showed a negative correlation to the OHIP-G14 (R = -0.283, Spearman's rho test p<0.01). For oral function also a negative correlation with OHIP-G14 was detected (Spearman's rho: -0.183). Conclusions: Patients with a prolonged dialysis vintage time show an improved OHRQoL, which might be mainly caused by the positive development of psychosocial pattern of OHRQoL. The oral health situation of HD patients seems unsatisfying, independently of dialysis vintage time and OHRQoL. Accordingly, an improvement in oral health situation of CKD5D patients is mandatory necessary. Thereby, consideration of psychosocial aspects especially at the beginning of CKD5D therapy and a sensitization regarding oral health issues with increasing vintage time might be recommendable. [ABSTRACT FROM AUTHOR]

Low nephron number may represent a major determinant of human primary hypertension in adult life. This hypothesis is supported by a genetic rat model, namely the Munich–Wistar–Frömter (MWF) rat, which demonstrates an inherited deficit in nephron number and the development of spontaneous hypertension. Insulin-like growth factor (IGF) I and II exert endocrine and paracrine effects that are required for normal growth and nephron development. We tested the hypothesis that low nephron number is already present during fetal development, and the expression pattern of important molecules of the IGF system is altered in MWF rat during the critical period of kidney development.

Secondary activation of the renin–angiotensin system plays a major role in the progression of chronic nephropathies, and blockade of endothelin (ET) receptors has been shown to confer nephroprotection in experimental models of proteinuric renal disease. We tested the nephroprotective potential of selective endothelin A receptor (ETA) and non-selective ETA and endothelin B (ETA/B) receptor blockade in the TGR(mRen2)27 transgenic rat model with renin-dependent hypertension (Ren2).

We evaluated the effects of angiotensin II subtype 1 (AT1) receptor antagonism on cardiac fibrosis and sarcoplasmic (SR) Ca2handling in a transgenic rat model of renin-dependent left ventricular (LV) hypertrophy (LVH).

AbstractThe aim of the present study was to analyze the hepatic endothelin system and its regulation in liver cirrhosis due to bile duct obstruction. Wistar rats were subjected for 6 weeks to: 1) sham operation; 2) bile duct obstruction; 3) bile duct obstruction and the selective oral endothelin A receptor antagonist LU 135252; 4) bile duct obstruction and oral silymarin, a hepatoprotective and antifibrotic compound. We determined tissue concentrations of endothelin-1 and big-endothelin-1 by ELISA and the density of both endothelin receptor subtypes in plasma membrane fractions by Scatchard analysis.The hepatic endothelin system in liver cirrhosis due to chronic bile duct obstruction is characterized by a simultaneous up-regulation of both endothelin-1 tissue concentration (7.2 fold compared to sham operation; p<0.001) as well as the density of both endothelin receptor subtypes (ETA7.4-fold, ETB4.9-fold, p<0.001, respectively) suggesting a synergistic activation of the hepatic endothelin system in this rat model of non-inflammatory cirrhosis. Treatment with proven antifibrotic agents such as silymarin or a selective endothelin-A-receptor blocker (LU 135252) did not reduce the activity of the hepatic endothelin system, suggesting that the hepatic endothelin system is not activated by the fibrotic process itself.

An inherited reduction in nephron number has been implicated in the development of salt-sensitive hypertension and end stage renal disease. The Munich Wistar Frömter (MWF) rat represents a genetic model with a 30–50 reduction of nephrons compared with normal rats. MWF rats develop spontaneous hypertension and increased urinary albumin excretion (UAE). We addressed the question whether the inherited defect in this model leads to salt-sensitive hypertension.

We used YC‐1 as a pharmacological tool to investigate the short‐term blood pressure effects of NO‐independent activation of sGC in normotensive and hypertensive rats. Four groups of normotensive Wistar‐Kyoto rats were treated by i.v. injection with vehicle (V), YC‐1 (YC‐1), sodium nitroprusside (SNP), or YC‐1 and SNP (YC‐1+SNP). Hypertension was induced in four additional groups of WKY rats by 3 weeks of oral treatment with L‐NAME. These animals were investigated with the same protocol as the normotensive animals: L‐NAME/V, L‐NAME/YC‐1, L‐NAME/SNP, L‐NAME/YC‐1+SNP. YC‐1 lowered mean arterial blood pressure (MAP) in normotensive and hypertensive animals similarly to SNP alone (P<0.05, respectively). The combination of YC‐1 with SNP caused a strong decrease of MAP in both the hypertensive and normotensive animals (P<0.05, respectively). SNP with YC‐1 also induced a pronounced cyclic GMP increase in the aorta. This study shows for the first time the blood pressure lowering potential of bimodal targeting of the NO‐sGC‐system.

The endothelins are 21-ammo-acid peptides which may play a role in the pathogenesis of hypertension. There is increasing evidence that the endothelins have a central function in mediating end-organ damage in hypertension, and that important effects of endothelin in the pathogenesis of hypertension may be based on the interactions of the endothelins and the renin-angiotensin and the nitric oxide systems.

We report the first case of a pregnant renal transplant patient with H1N1/09 infection. The woman showed a mild clinical course after diagnosis of H1N1/09 infection and therapy with oseltamivir (2×45?mg per day). After delivery by cesarean section, the neonate exhibited moderate respiratory and circulatory dysregulation, which spontaneously normalised a few days postpartum. In conclusion, rapid diagnosis of H1N1/09 and dose-adapted therapy with oseltamivir resulted in successful delivery of a healthy infant in our renal transplanted patient but emphasized the need for consequent vaccination strategies in pregnant transplant recipients for new influenza A pandemics in the future.

The pressure-activated cation channel (PAC), a novel type of mechanosensitive channel, has been suggested to act as a mechanosensor in aortic endothelium. In experimental hypertension, PAC function was up-regulated in the established phase of high blood pressure. This association of altered PAC function and elevated arterial pressure suggests that PAC function is regulated by alterations in blood pressure. In the present study, we electrophysiologically investigated PAC function in intact endothelium of aorta (EA) and mesenteric artery (EMA) from stroke-prone spontaneously hypertensive rats (SHRSP), SHRSP after 4 weeks of treatment with quinaprilat (10 mg/kg/day), and normotensive Wistar-Kyoto (WKY) rats. In untreated SHRSP and WKY rats, systolic blood pressure (SBP) was 201 ± 3 mm Hg and 142 ± 3 mm Hg, respectively. In quinaprilat-treated SHRSP, SBP was lowered to 135 ± 5 mm Hg. Apparent PAC density (percentage of patches with PAC activity) in EA of untreated SHRSP (63.7% ± 7.3%) was 2.4-fold higher than in WKY rats (26.0% ± 5.0%). In contrast, no significant PAC up-regulation was detected in EMA of SHRSP (15.7% ± 4.2%) compared with WKY rats (12.0% ± 3.9%). In EA of quinaprilat-treated normotensive SHRSP, PAC density (27.1% ± 5.2%) was lowered to levels found in normotensive WKY rats. Unitary conductance and pressure sensitivity of PAC were not altered in either hypertensive or normotensive rats. Taken together, hypertension-induced increases of endothelial PAC density can be completely reversed by antihypertensive therapy. The PAC up-regulation in EA was interpreted as a compensatory mechanism to enhance Ca2+-influx and subsequently the synthesis of vasodilatory factors. This mechanism is missing in EMA of SHRSP, which might contribute to high blood pressure in this rat model of severe genetic hypertension. Am J Hypertens 2001;14:716–721 © 2001 American Journal of Hypertension, Ltd.

Circulating plasma endothelin1 ET1 is elevated in liver cirrhosis, in a diseasestagedependent manner. However, ET1 exerts its effects mainly via paracrine and autocrine pathways. Therefore, the aim of the present study was to analyze the hepatic endothelin ET system in liver cirrhosis resulting from bile duct obstruction BDO. Wistar rats were subjected for 6 weeks to either sham operation control or BDO. Thereafter, hepatic ET1 concentrations were elevated 7.2fold in BDO compared to control p < 0.001, whereas big ET1 was unchanged. The density of both ET receptor subtypes was upregulated in BDO ETA7.4fold and ETB4.9fold vs control, p < 0.001, respectively. The affinity of both receptor subtypes was significantly reduced in BDO. In conclusion, our data demonstrated for the first time that the hepatic ET system in liver cirrhosis is characterized by a simultaneous upregulation of both ET1 tissue concentration as well as the density of hepatic ETAand ETBreceptors, suggesting a synergistic activation of the hepatic ET system in rats with BDO. The increased ET1 tissue concentration is not a result of an altered big ET1 synthesis in biliary liver fibrosis, suggesting an increased activity of endothelinconverting enzyme ECE in liver cirrhosis.

Circulating plasma endothelin1 ET1 is elevated in liver cirrhosis, in a diseasestagedependent manner. However, ET1 exerts its effects mainly via paracrine and autocrine pathways. Therefore, the aim of the present study was to analyze the hepatic endothelin ET system in liver cirrhosis resulting from bile duct obstruction BDO. Wistar rats were subjected for 6 weeks to either sham operation control or BDO. Thereafter, hepatic ET1 concentrations were elevated 7.2fold in BDO compared to control p < 0.001, whereas big ET1 was unchanged. The density of both ET receptor subtypes was upregulated in BDO ETA7.4fold and ETB4.9fold vs control, p < 0.001, respectively. The affinity of both receptor subtypes was significantly reduced in BDO. In conclusion, our data demonstrated for the first time that the hepatic ET system in liver cirrhosis is characterized by a simultaneous upregulation of both ET1 tissue concentration as well as the density of hepatic ETAand ETBreceptors, suggesting a synergistic activation of the hepatic ET system in rats with BDO. The increased ET1 tissue concentration is not a result of an altered big ET1 synthesis in biliary liver fibrosis, suggesting an increased activity of endothelinconverting enzyme ECE in liver cirrhosis.